Ribosomal proteins, classically thought to function only as translational machinery, now appear to play a role in the HDM2-p53 pathway. Recent work by scientists at the University of Texas MD Anderson Cancer Center in Houston shows that during cell-growth inhibition, ribosomal protein L11 translocates from the nucleolus to the nucleoplasm where it binds HDM2 (human double minute 2), disrupting HDM2's contact with tumor suppressor p53.[1] Without HDM2-mediated p53 ubiquitination, p53 is no longer targeted for degradation; thus it is free to induce cell-cycle arrest.